For several centuries marijuana was utilized as an analgesic for pain relief. Up until the 1940’s marijuana was a legal substance and often used to alleviate a variety of ailments—much like the advocates of the use of medical marijuana are saying today. The federal government of the United States classifies marijuana as a high risk substance. Yet the proponents of medical marijuana state that it is rarely an addictive drug. In addition, there has never been a death by overdose on cannabis!One of the medical areas that have benefited the most has been with Alzheimer’s patients. This form of dementia can leave an individual trapped in a healthy body with a memory that spans previous decades but can’t remember the most recent of events. The regression is gradual with an individual first feeling ‘forgetful’ yet it is much more than just forgetting where one left their car keys—it’s more of an inability to recognize how those keys are used. Eventually, the disease also takes the healthy body and turns it into a shell of its former self. Many times Alzheimer’s victims lose their appetite, or even forget how to feed themselves at the most severe stages.On any given Alzheimer’s ward at a nursing home, you can see patients walking up and down the corridor hundreds of times during the course of the day. As, the disease progresses, they will get to the end of the corridor and just stand there—forgetting that they need to turn around! There is even a time of day when this activity becomes more active—it’s when the sun starts to set and is referred to clinically as ‘sun downing’. The patient is nervous, very agitated, can become aggressive or very emotional. Individual studies have found that when a patient drinks a tea made from the marijuana leaves that their agitation dissipates and they are able to settle down for a peaceful evening. Their whole mood changes. Their appetite increases and meal time is no longer a fight to get some nourishment in to them.As a result of studies done by scientists at Madrid’s Complutense University they were able to publish in the Journal of Neuroscience that cannabinoids, a compound found in marijuana, reduces the ‘pathological processes’ associated with Alzheimer’s disease. It appears that there may be a strong link to these cannabinoids that can help with new drug development. Apparently, the cannabinoid receptors that we all have in our brains were much lower than those with healthy brains. These cannabinoid receptors work in conjunction with microglia cells to keep the immune system healthy. When these cells perceive themselves to be under attack, they cause an inflammation in the brain. The introduction of cannabinoids prevents that inflammation from taking place.Medical Marijuana has not been proven to improve one’s short or long term memory, many would argue it is destructive to one or both, but it clearly has a positive effect on the disease of Alzheimer’s. First, it can delay the progression of the disease by preventing the inflammation to take place within the brain. Second, it can help with weight gain since food refusal is a very big problem for those with Alzheimer’s. Third, it helps with easing the symptoms of depression, acting as a mood enhancer. And fourth, it can ease that sense of agitation and aggressive behavior that often goes hand in hand with the disease.

Hmm, this might explain quite a bit. Alzheimer's disease doesn't seem to be common among populations that have a diet high in omega-3 fatty acids, gained through eating seafoods or vegetables (a lot of veggies like spinach, broccoli, flax seeds, walnuts, etc. are rich in ALA, which then can be converted in the liver, albeit poorly, to DHA). One more thing that deserves mention is that omega-3 fatty acids are strong anti-inflammatory agents and moderate an immune response. I wonder if this would also contribute to other beneficial effects for the brain, especially in those afflicted with Alzheimer's.

One more thing that deserves mention is that omega-3 fatty acids are strong anti-inflammatory agents and moderate an immune response. I wonder if this would also contribute to other beneficial effects for the brain, especially in those afflicted with Alzheimer's.

I found this on inflammation and Alzheimer's:

Professor Jeffrey Kelly of the Scripps Research Institute has recently proposed that inflammation could be start of a chain reaction that leads ultimately to Alzheimer's disease. Normal brain molecules are disrupted as a result of inflammation and this can cause amyloid beta proteins in the brain to misfold. Misfolded amyloid beta proteins are thought to have a critical role in the development of Alzheimer's.According to Kelly the inflammation process might occur years before the onset of Alzheimer's and be the result of any number of infections people can contract.

The anti-inflammatory properties of omega-3 fatty acids are apparently due to their ability to decrease the production of prostaglandins by competing with omega-6 fatty acids for binding sites thereby reducing the amount of omega-6 that can be converted to prostaglandins.

The anti-inflammatory properties of omega-3 fatty acids are apparently only beneficial for those with Alzheimer's during early stages of the disease:

"The mechanisms by which omega-3 fatty acids could interfere in Alzheimer's disease pathophysiologic features are not clear, but since anti-inflammatory effects are an important part of the profile of fish oils, they are conceivable also for Alzheimer's disease," the authors write. This could potentially explain why effects were seen only in those with very early-stage disease--recent evidence suggests that there is a critical period two or more years before patients develop dementia when levels of chemicals that signal the presence of inflammation are elevated. "It is possible that when the disease is clinically apparent, the neuropathologic involvement is too advanced to be substantially attenuated by anti-inflammatory treatment."

Curcumin and Alzheimer’s Disease. Our group has tested curcumin in several models for Alzheimer’s and found that it not only reduces oxidative damage and inflammation (as expected), but also reduces amyloid accumulation and synaptic marker loss and promotes amyloid phagocytosis and clearance. Curcumin worked to prevent synaptic marker and cognitive deficits caused by amyloid peptide infusion and abeta oligomer toxicity in vitro.

Silly old herbs to the rescue yet again! (see maleria)I love it.I tried to grow some from a root bought at woolworths (supermarket) without any luck.I will try again now.

Curcumin- major source turmeric , (a curry spice that grows a bit like ginger) is popping up a lot in medical research these daysEGCurcumin has anticancer effects

Curry powder is a mixture predominantly composed of turmeric root extract and other spices such as coriander and fenugreek.

Curcumin, a turmeric root extract, has been shown to possess activity in the treatment and prevention of cancer, multiple sclerosis, and Alzheimer's disease. The molecular mechanism for its anticancer effect is largely unknown, although it is thought to inhibit the synthesis of MDM2, an oncoprotein known to bind p53 and modulate p21 expression.

There is a very exciting study going on in Australia.I am going to try and add an ABC podcast to this link ( unfortunately the cash starved ABC -pollies. of all ilk hate it-only keeps radio shows for 4 weeks)

Hopefully there is an audio file here on Alzheimer's and testosterone.Worth a listenVery current research.

NO?I'll ask for help

meanwhileprions seem to be important

Professor Hooper concludes: "Until now, the normal function of prion proteins has remained unclear, but our findings clearly identify a role for normal prion proteins in regulating the production of beta-amyloid and in doing so preventing formation of Alzheimer’s plaques.

TSE and other prion diseases are sometimes transmissible between different species, as seen with the unfortunate BSE and vCJD syndromes in Europe. Prions, it seems, were transmitted through sheep (scrapies) --> cattle (BSE) --> and humans (vCJD) because of the similarity of the native brain protein in all of these species. To my understanding, animals which have PrP that is dissimilar enough to avoid the "misfolding" and "transmission" that BSE prion proteins can induce are either highly resistant to TSEs or immune to it, because their proteins cannot be "messed up" by the prion proteins from other species. (This doesn't mean that they are immune to their own prion diseases, though. It's just another example of the difficulty facing diseases when they try to jump the "species barrier.")

Now to tie the explanation above with your link, this is directly relevant to the research because scientists have replicated a similar cross-species transmission process in a favorite test organism, yeast, and another fungi. Yeast possess a protein similar to prion protein in animals and can suffer from some of the effects of TSE-like prion diseases, where their proteins misfold, clump, and cause malfunction in the organism. Being able to reproduce and study the transmission of prion diseases allows for greater understanding and future treatments, especially when we understand better how prions work in such a "simple" model organism as yeast. Scientists really like simple, cheap, understandable models for obvious reasons.

"We used to think that Alzheimer's disease was a problem with the production of too much amyloid-beta, but it's become clear in recent years that the problem is with faulty clearance of amyloid-beta," said Zlokovic, professor of Neurosurgery and Neurology and director of the Frank P. Smith Laboratory for Neuroscience and Neurosurgery Research. "We aren't really talking about massive amounts of amyloid-beta. Even a small malfunction in the elaborate system that carries it into or out of the brain could lead, over years, to accumulate in amounts that damage the brain."

. . .Zlokovic's group decided to try to reduce amyloid-beta levels in the body by synthesizing an altered, super-potent form of sLRP that binds amyloid-beta more efficiently than natural sLRP. In blood samples from patients with Alzheimer's disease, the modified version of sLRP, known as LRP-IV, soaked up and virtually eliminated amyloid-beta.

The compound had an even more dramatic effect in mice with features of Alzheimer's disease: LRP-IV lowered the levels of amyloid-beta in their brains by 85 to 90 percent. The mice that received the compound also had improved learning and memory compared to mice that did not receive LRP-IV, and they had 65 percent more blood flow in their brains in response to brain stimulation -- a flick of their whiskers. . .The team is now working with a company created by Zlokovic, Socratech, to create a form of LRP-IV that could be tested in people. Zlokovic hopes to have such a product ready for testing within two years..

Women could stop bothering to prepare meals as dementia sets in.GettyResearchers have found a simple physical symptom that accompanies the early, subtle brain changes that lead to dementia. Women who will go on to develop dementia begin to lose weight at least ten years before diagnosis, say researchers at the Mayo Clinic in Rochester, Minnesota.

While the symptom of weight loss is too common to serve as a usable early warning sign for mental decline, researchers hope other such physical changes could be used to spot dementia before memory loss sets in.

David Knopman, who led the study published in Neurology1 today, thinks the women may have shed the weight because creeping damage in their brains caused them to lose interest in food. He speculates that the disease could cause apathy or dull the senses of taste and smell, making food less appealing.

Neurologists have long suspected that conditions such as Alzheimer's disease begin to develop 10-20 years before diagnosis. But spotting such early changes has proven difficult. This is one of only a few studies to make a link between physical symptoms and emerging dementia.

Another example is memantine, our newest tool in the struggle against Alzheimer's disease. This drug appears to be effective because it has a low affinity for the N-methyl-D-aspartate (NMDA) glutamate receptor. Because it has only a low affinity, it only has an effect when the glutamate system is hyperactive and potentially neurotoxic, so it slows the progression of cell death in Alzheimer's disease. This is in stark contrast to drugs that have a high affinity for the NMDA glutamate receptor, such as ketamine or dextromethorphan, which can interfere with the overall functioning of the glutamate system and in some cases mimic schizophrenia to the point of precipitating psychosis.

PS Yet another very preventable reason.Public Dental care in Australia is a disgrace with a 12 month waiting list for "emergencies" and a 2-3 year wait for any other work!

According to researchers in the U.K., older people who have lost all their teeth are more than three times more likely to develop memory problems and dementia than those who still have teeth left.

The study’s lead author, Dr. Robert Stewart of Kings College London, admits this study raises more questions than it answers, and that at this point they are not able to say what causes what. However, he states the take-home message is, “Particular attention may need to be paid to the health and nutrition of people with cognitive impairment because they may also have dental problems.”

A lot of research now focuses on the associations between diet and dementia, especially Alzheimer’s. But poor dental health may also boost your risk of cognitive problems, because:

1.

Dental disease often causes prolonged inflammation and infection in your mouth, which may alter some factors in your blood, possibly causing problems in your brain. 2.

People who lose their teeth tend to alter their diet. A less balanced diet can result in vitamin deficiencies and other problems that might alter or affect brain function.

Journal of the American Geriatrics Society September, 2007; 55(9):1410-4

And still another study listed 22 different categories of drugs that can cause symptoms that mimic Alzheimer's... plus 14 different over-the-counter drugs that can cause those symptoms!

Here's a typical scenario. A healthy person goes to the doctor for a checkup and is told his cholesterol or blood pressure is high. So he starts taking medication, which causes side effects. This leads his doctor to give him a second drug to treat those side effects. But, of course, that second drug causes new side effects. So the doctor prescribes a third drug to treat the side effects of the second one!

The tree bark compound, known as gambogic amide, behaves much like Nerve Growth Factor (NGF), a molecule found in the brain. NGF binds to TrkA, a neuronal receptor, and activates neuronal signaling. It is known that the loss of TrkA density correlates with neuronal atrophy and severe cognitive impairment such as that associated with Alzheimer's disease.

Because gambogic amide also binds to TrKA and activates neuronal signaling, the researchers believe it may have potential as a therapeutic treatment in people affected by neurodegenerative disease, such as stroke, Alzheimer's disease and peripheral diabetic neuropathies.

Gambogic amide is derived from gambogic acid, a major ingredient of gamboges, a brownish-orange resin exuded from the Southeast Asian Garcinia hanburryi tree. The resin has been used in that area of the world for thousands of years to treat cancers without any reported toxicity to noncancerous cells.

Diet, exercise and drugs like allopurinol (all of which lower UA levels) could eventually be of value in reducing this risk, especially for those with additional risk factors such as diabetes, obesity and hypertension, the researchers say. But they caution that it would be premature to try this now.

In a study published in the Oct. 2 issue of Neurology, lead author David Schretlen, Ph.D., of the Department of Psychiatry at The Johns Hopkins University School of Medicine, linked UA levels to high volumes of so-called white matter hyperintensities (WMH), which are small dead areas of the brain that occur when brain cells are deprived of oxygen. Lack of oxygen due to clots or burst blood vessels in the brain are hallmarks of classic large strokes.

"Over a lifetime, it is common to have a small number of these mini strokes and not even notice," says Schretlen, "but as the overall volume of WMH increases, the damage can seriously disrupt how quickly we think and how effectively we learn and remember information."

The role of UA is best known in gout, where buildup of the fatty acid creates pain and disability in the feet and toes. However, UA appears to play contradictory roles in the brain, says Schretlen. For example, UA is a powerful antioxidant that might even protect against Parkinson disease and Alzheimer disease, possibly because antioxidants destroy oxygen free radicals that damage tissue.

On the other hand, elevated UA accompanies diabetes, obesity and heart disease, and it is a well-known risk factor for stroke. One possible explanation of its seemingly contradictory nature is that, like a double-edged sword, UA is beneficial, but processes leading to its production can be harmful under some circumstances, says Schretlen.

Don't you hate these pre-emtive press releases?"Discovered the cure to Alzheimer's"(maybe perhaps in 20 years- if you give us lots of money for our research and BMWs.) So many science press releases are like this.

Alzheimer's cold sore virus linkCold soreThe cold sore virus has been linked to Alzheimer's diseaseEvidence is building that the cold sore virus may be linked to Alzheimer's disease, an expert says.

In lab tests, Manchester University found brains infected with the herpes simplex virus, HSV-1, saw a rise in a protein linked to Alzheimer's.

Scientists believe the discovery could pave the way for a vaccine that may help prevent the brain disorder, New Scientist magazine reported.

But such a breakthrough was a long-time off, experts said.

We need to carry out much more work into this, but the problem is people are quite sceptical of a viral linkDr Ruth Itzhaki, of Manchester University

The researchers infected cultures of human brain cells with the virus and found a "dramatic" increase in levels of the beta amyloid protein - the building blocks of deposits, or plaques, which form in the brains of people with Alzheimer's